An understanding of the mechanism whereby polynuclear aromatic hydrocarbons (PAH) and other environmental pollutants elicit an atherogenic response in the chicken would be valuable in determining the feasibility of using the chicken as a possible model for the study of pollutant induced or accelerated atherogenesis. Chickens spontaneously develop atherosclerotic disease and the early stages of plaque formation in the chicken are quite similar to those in man. Results recently obtained in our laboratory indicate that chickens treated with PAH's develop large, focal intimal plaques in the abdominal aorta. There is also evidence that carbon monoxide (CO) and carbon disulfide (CS2) may be contributing factors to cardiovascular disease in a variety of species, including man. A systematic study of dose and time of treatment on plaque induction and intimal cell proliferation in chicken aorta will be made for 7, 12 dimethylbenzanthracene (DMBA) which was a potent atherogen in our preliminary study. In addition, benzo(a)pyrene (B(a)P), the most commonly studied PAH, dibenz (a,h) anthracene and dibenz (a,c) anthracene will be tested for comparative atherogenicity in the chicken. Evidence will be sought, through the use of 3H-labeled PAH's, that these compounds are taken up directly in the aorta. The binding of the aqueous-insoluble PAH's to serum lipoproteins will be investigated as a possible mechanism of solubilization and transport of the PAH's to the arterial wall. The artherogenic potential of injected cigarette tar and of inhaled CO and CS2 will be tested in a series of pilot experiments.